Student research project
Supervisor(s): Dr Brian Drew and Simon Bond
Obesity is a strong risk factor for many chronic illnesses including diabetes, cardiovascular disease and cancer. However, there is a small proportion of people who are obese, that have no clinically detectable metabolic defects and live otherwise normal lives. These so-called metabolically healthy obese individuals, appear to have a genetic advantage to deal with obesity and are for the most-part refractory to the usual complications that are associated with obesity. One of the candidate hypotheses for this protection, is a greater ability for these people to store their fat in peripheral fat depots (subcutaneous white adipose tissue — sWAT), and not in fat depots that are close to our vital organs (visceral WAT — vWAT).
Over the past decade there has been a significant body of research investigating the genetic pathways that control whether an individual stores their fat in sWAT or vWAT, which has pointed to pathways important for the control of mitochondrial activity. Subsequent studies have shown that by genetically reducing mitochondrial activity in adipose tissue, the WAT becomes unhealthy and unable to store fat properly. On the flip side, studies that genetically activate mitochondria in adipose tissue lead to healthy WAT, particularly sWAT, which has an enhanced ability to store fat and thus protect the rest of the body from lipotoxicity (fat build up).
Thus, we currently have several ongoing studies in our lab that aim to investigate the therapeutic benefit of activating mitochondria in WAT and promoting the formation of healthy WAT, with the aim of identifying new drug targets to prevent complications from obesity.
This project is suitable for an Honours or PhD student.